We investigated the relationship between perfusate concentration of glucose and its utilization and lactate production derived from exogenous glucose and from metabolism of endogenous substrates. Isolated rat lungs were ventilated with 5% CO2 in air and perfused for 100 min with Krebs-Ringer bicarbonate buffer containing 3% bovine serum albumin, 10(-2) U/ml insulin, [U-14C]glucose and [5-3H]glucose. Glucose utilization, total lactate production, [14C]lactate production, and 3H2O production were measured. The apparent Km and Vmax for glucose utilization were 3.4 mM and 72.5 mumol/g dry wt per h, respectively. Lactate production from endogenous substrates, calculated as the difference between total and [14C]lactate, was 37.6 +/- 2.2 mumol/g dry wt (n = 36); it was unaffected by perfusate glucose concentration and by omission of insulin, but increased threefold with anoxia. Lactate production from 1.5 mM glucose was significantly less (P less than 0.02) with insulin omitted. Glycogen content was unchanged during perfusion without glucose. These results suggest that: 1) protein catabolism contributes to lung lactate production; 2) glucose utilization by lung is not maximal at resting physiological glucose concentrations; and 3) insulin is required at low glucose concentrations for maximal glycolytic rates.

Specific activity curves of expired air were obtained after the injection of NaHC14O3 into normal and alloxan diabetic rats in the postabsorptive and fasted state. The curves were analyzable into three constituent simple exponential functions. This suggested a pool system with three conjoined compartments. The rate of CO2 output being known, pool sizes and rates of carbon movement could be calculated by mathematical treatment of slopes and intercepts. The primary space within which injected C14 equilibrated very rapidly was treated as a single complex pool. Its size was compatible with that of extracellular fluid. Two side-pools were included in the model. The slower moving one had a rate of turnover and size which were greater in the fasted than in the postabsorptive state. This suggests that organic carbon participates in the HCO3– interchange and that CO2 fixation is increased during fasting. No systematic differences between normal and diabetic animals were encountered.

Nutritional, chemical and metabolic studies have been carried out on hereditarily muscular dystrophic mice and their littermate controls. Certain characteristics of the dystrophic syndrome which may not have been emphasized previously are described: denudation of the eyelids, periocular inflammation, tremors and an unusual reflex involving the head and neck, inflammation of the penis, and diminished bone growth. The dystrophic mice consumed, on the average, more food per day per unit body weight than their normal controls. Parenteral administration of vitamins A, D, E, the B-complex vitamins and ascorbic acid failed to reverse any of the dystrophic syndrome in eight dystrophic mice. The metabolic rate was normal (per unit weight basis) as measured by the rate of CO2 production; similarily, acetate-1-C14 was oxidized to C14O2 at the same rate in normal and dystrophic mice. Finally, levels of plasma glucose, cholesterol, protein-bound I131, and of liver cholesterol were not significantly different in a small group of normal and dystrophic mice.

The formation of oxidation products of unsaturated fatty acids in homogenates of muscle, heart, kidney, brain and liver was studied by means of the thiobarbituric acid assay. Tissues from mice having a hereditary myopathy did not show a regular, significant increase in the formation of ‘fatty acid peroxides’ over that of normal tissues.

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